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Nox4-dependent ROS production is involved in CVB3-induced myocardial apoptosis

Jinyu Chi1, Shouxian Yu1, Chunnan Liu1

  • 1Department of Cardiology, First Affiliated Hospital of Harbin Medical University, No. 199 Dazhi Street, Harbin, 150001, China.

Biochemical and Biophysical Research Communications
|July 30, 2018
PubMed

Insights

The study found that Nox4, a NADPH oxidase homologue, is upregulated in viral myocarditis. Inhibiting Nox4 reduced disease severity and myocardial apoptosis, suggesting its role in Coxsackievirus B3 infection.

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Virology

Background:

  • Viral myocarditis is a serious cardiovascular disease with unclear mechanisms.
  • Coxsackievirus B3 (CVB3) is a primary cause of viral myocarditis.
  • NADPH oxidase gene expression increases during CVB3 infection.

Purpose of the Study:

  • To investigate the role of Nox4, a NADPH oxidase homologue, in CVB3-induced viral myocarditis.
  • To determine if Nox4 contributes to myocardial apoptosis during CVB3 infection.

Main Methods:

  • Assessed Nox4 expression in a mouse model of CVB3 infection and in vitro cell cultures.
  • Administered DPI, a Nox4 inhibitor, to infected mice.
  • Measured intracellular reactive oxygen species (ROS) release and apoptosis in vitro.

Main Results:

  • Nox4 expression was elevated in viral myocarditis models (in vivo and in vitro).
  • DPI treatment improved CVB3-induced myocarditis in mice.
  • DPI inhibited intracellular ROS production and apoptosis in vitro.

Conclusions:

  • Nox4 is upregulated during CVB3 infection and contributes to viral myocarditis.
  • Nox4-dependent ROS production plays a role in CVB3-induced myocardial apoptosis.
  • Targeting Nox4 may offer a therapeutic strategy for viral myocarditis.

Keywords:
ApoptosisCVB(3)Nox4ROSViral myocarditis

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